Dear editor
We have read the article titled “ROCK2 and MYLK variants under hypobaric hypoxic environment of high altitude associate with high altitude pulmonary edema and adaptation” by Pandey et al1 with profound interest. The authors have reported an association of rho-associated coiled-coil kinase isoform 2 (ROCK2) and myosin light chain kinase (MYLK) with high-altitude pulmonary edema (HAPE) in the Indian population. As per the Lake Louise Consensus on the definition and quantification of altitude illness, HAPE is diagnosed by presence of at least two of the symptoms such as dyspnea at rest, cough, weakness or decreased exercise performance, chest tightness, or congestion; and at least two of the signs such as rales or wheezing in at least one lung field, central cyanosis, tachypnea, and tachycardia, in the background of recent gain of altitude.2 The authors have used a detailed medical examination for these subjects and have recorded the mandatory clinical findings for HAPE. They have described findings of mean arterial pressure and peripheral capillary oxygen saturation but have inadvertently not reported the resting heart rate and respiratory rate of their subjects. The reporting of these clinical parameters (especially tachypnea and tachycardia) would have fulfilled all the criteria required for the diagnosis of HAPE. The authors have also mentioned that an exhaustive questionnaire was used for the diagnosis of HAPE. As physiologists with interest in the field of high-altitude (HA) medicine, we are interested in knowing the details of this questionnaire.
The authors of this study have also ruled out the presence of acute mountain sickness (AMS) by using the Lake Louise Questionnaire only in HAPE control subjects but not in HAPE–susceptible ones, which is not understandable as AMS and HAPE are two distinct HA-related acute illnesses occurring because of the involvement of two different physiological systems, the central nervous system and the pulmonary system, respectively.3 If uniformity of ascent and rest (or exercise) after entry is assumed, the likelihood of occurrence of AMS in both controls and HAPE-susceptible subjects remains the same.4
The authors have concluded by reporting a role of ROCK2 and MYLK in determining the susceptibility of an individual to HAPE, but practical application of this outcome in the field of HA medicine remains obscure. HAPE is a rare disease, as acknowledged by the authors, and has an incidence of only 0.31% among Indian male lowlanders after an acute ascent (by air) to an altitude of 3,400 m in the Western Himalayas.5
Footnotes
Disclosure
The authors report no conflicts of interest in this communication.
References
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